X-linked B-lymphocyte Defect in CBA/N Mice. III. Abnormal Development of B-lymphocyte Populations Defined by Their Density of Surface Immunoglobulin

CBA/N mice have an X-linked defect in B-lymphocyte function characterized by a failure to respond to certain thymus-independent antigens. When studied by rapid flow microfluorometry, adult CBA/N splenic B lymphocytes labeled with either fluorescein-conjugated (Fl) anti-Ig or Fl anti-mu had fluorescence profiles which were considerably different from those of B lymphocytes derived from normal mice. By studying progeny of crosses of CBA/N and normal mice, it was shown that the abnormal fluorescence profiles of CBA/N B cells were determined by an X-linked gene. The fluorescence profile of adult CBA/N splenic B lymphocytes labeled with anti-mu were very similar to the patterns of neonatal normal and of neonatal CBA/N splenic B lymphocytes suggesting that the defect of CBA/N mice is due to a failure in the development of a mature B-lymphocyte population. The fluorescence profiles of adult CBA/N splenic B lymphocytes labeled with Fl anti-Ig also had immature characteristics in that the frequency of cells with large amounts of surface immunoglobulin was increased in comparison to that of normal strains and the population of cells with low-to-intermediate density of total surface immunoglobulin, which appear characteristic of normal adult splenic B lymphocytes, was markedly diminished.